Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat hepatocellular carcinomas (HCCs) induced by aflatoxin B1 (AFB) treatment were examined for changes in the p53 tumor suppressor gene and in p53 suppressor gene expression. A high proportion of HCCs (nine of 11 tumors in six of eight animals) exhibited new p53 restriction fragments, indicating genomic alterations of one of the p53 alleles. Each tumor with an altered p53 restriction-fragment pattern exhibited a new fragment in one of two size classes (3 kb or 7 kb with EcoRI digestion) that were missing portions of the 3' end of the p53 gene. These findings indicate that apparently similar genomic rearrangements or deletions occurred independently in AFB-induced tumors. When compared with nontumor liver tissue from the same animal, the tumors with p53 gene alterations showed dramatically reduced levels of p53 mRNA and protein and greatly increased levels of histone H2B and retinoblastoma tumor suppressor (Rb) mRNA. In two HCCs showing no evidence of p53 restriction-fragment alterations, mutant p53 protein was detected. Mutant protein was also detected in two liver samples containing an adenoma and altered foci. These data suggest that alterations of the p53 tumor suppressor gene are involved in the induction of rat HCC by AFB.
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PMID:Alterations in the structural gene and the expression of p53 in rat liver tumors induced by aflatoxin B1. 135 44

Degenerations (atrophies) of the retina are divided into primary (hereditary) and secondary forms including glaucomatous retinopathy of retinal atrophy. The pathogenesis of inflammation of the retina is considered. This condition generally appears in association with inflammation of the choroid (chorioretinitis), but can also occur as an isolated inflammatory condition during infectious disease (distemper). The functional conditions for retinal detachment, its rhegmatogenous and nonrhegmatogenous types, as well as the consequences of retinal detachment are described. Comparison of the pathology of retinal tumors shows that retinoblastoma is not known in animals. However, neuroepithelial tumors like the so-called acquired adenoma and adenocarcinoma of the mature ciliary epithelium as well as the rare congenital tumors of the embryonic neuroepithelium i.e. the medulloepithelioma and the ganglioneuroma are seen in animals. Finally, the rare but not unusual parasitic retinopathies are mentioned.
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PMID:[Pathology of the retina]. 144 May 98

Bilateral tumors of the same histotype occur rarely in opposite organs. These include hereditary diseases such as retinoblastoma and Wilm's tumor. Bilateral tumors of the same histotype also occur in the parotid glands. A study was performed to determine if there is a possibility that hereditary tumors are included in such cases. Two cases of bilateral parotid tumors, one of pleomorphic adenoma and one of adenolymphoma were reported, and 59 cases reported between 1942 and 1990 with clear times of onset which underwent histological examinations were analyzed. The main histotypes were adenolymphoma in 50.8% (30 cases), pleomorphic adenoma in 27.1% (16 cases), acinic cell tumor in 13.6% (8 cases). Onset of the tumors was simultaneous in 43% of the adenolymphomas. The sex and age at onset showed the same trends as in unilateral cases for each histotype. Among parotid tumors, the percentage of bilateral onset is 1-2%, and when adenolymphomas which show the highest incidence among such tumors were considered from the standpoints of multiplicity, simultaneous onset and the fact that they are benign, the possibility that hereditary diseases are included in the aforementioned 43% was suggested.
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PMID:[Hereditary study on bilateral parotid tumors of the same histotype]. 164 69

Neuroepithelial tumors of the ciliary body occur more seldom than retinoblastoma. The congenital form is called medulloepithelioma, the adult-acquired adenoma or adenocarcinoma. Medulloepitheliomas consist of organoid epithelial structures developing anteriorly along surfaces such as the iris. The authors report on a congenital type unusually growing not only anteriorly along the lens, but also posteriorly along the retina's surface causing retinal detachment.
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PMID:Medulloepithelioma of the ciliary body. 192 27

Chromosome abnormalities found in pediatric solid tumors include deletions, translocations, homogeneously staining regions (hsr)/double minutes (dms), and ploidy abnormalities. The discovery of a 13q14 deletion found in lymphocytes of patients with retinoblastoma and developmental delay has led to the cloning of the retinoblastoma gene. Likewise the discovery of an 11p13 deletion in lymphocytes of patients with Wilms' tumor and aniridia has led to the cloning of the Wilms' tumor gene. Chromosome deletions found in tumor cells are considered to play a role on the homologous deletion of cancer suppressor genes. Recently, various translocations have been found mostly in soft tissue sarcomas; i.e. t(11;22) in Ewing's sarcoma, t(2;13) in alveolar rhabdomyosarcoma, t(3;8) in pleomorphic adenoma, t(3;12) in lipoma, t(12;16) in liposarcoma, t(12;14) in leiomyosarcoma, and t(X;18) in synovial sarcoma. These translocations provide important information on the difficult diagnosis of soft tissue sarcomas, and on the selection of chemotherapy protocol. Tumor cells in advanced stage neuroblastomas often show hsr/dms, in which N-myc amplification occurs. While near triploidy was regularly found in early-stage neuroblastomas, near-diploidy or near-tetraploidy was usually found in advanced stage tumors. Among various prognostic factors, N-myc copy numbers and tumor cell ploidies had the largest influence on the prognosis of neuroblastoma patients. Cytogenetic and molecular genetic analyses on tumor cells are becoming increasingly important for the diagnosis of pediatric solid tumors, and the prediction of the patients' prognosis.
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PMID:[Cytogenetics in pediatric solid tumors]. 217 98

Molecular genetic studies of tumor-specific allele loss, originally associated primarily with research regarding childhood hereditary cancers such as retinoblastoma and Wilms' tumors, only lately have been recognized as a relatively fast and fruitful way of locating cancer genes on human chromosomes. To date, over 25 different cancers have been tied to a gene (or genes) on a specific chromosome when this method has been used. During the past year alone, this approach has permitted detection of three genes involved in either hereditary or sporadic colorectal cancers. These three genes, located on chromosomes 5q, 17p, and 18q, are believed to belong to the newly described tumor suppressor (or growth suppressor) gene class, whose effects are opposite those of activated cellular oncogenes, which promote uncontrolled cell growth. Present studies, however, have not shown losses of any of these tumor suppressor genes to be correlated with the presence of activated ras genes in colorectal adenomas or carcinomas. During progression from adenoma to carcinoma, ras gene mutations and 5q allelic deletions are likely to be earlier events, whereas allelic losses from chromosomes 18q and 17p seem to occur more often in advanced tumors. Involvement of the genes on 5q (FAP) and 18q (Lynch syndrome II) in hereditary colon cancer syndromes is supported by linkage studies, but their respective roles (as well as that of the gene on 17p) in familial and sporadic colorectal cancer remain to be precisely defined. Probable isolation of these three genes by molecular cloning within the next few years will help elucidate their specific biologic functions. It will also permit early detection, and thus prevention, of some familial colon cancers (such as FAP), and possibly allow DNA marker-based separation of different colon cancer subtypes of similar histologic appearance.
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PMID:Molecular genetic studies of colon cancer. 264 66

A survey of 2704 eyes with intraocular tumors in patients who were evaluated on the Oncology Service at Wills Eye Hospital showed that 126 of the tumor-containing eyes (5%) had tumor-induced elevated intraocular pressure (IOP) at the time of diagnosis of the tumor. Of the 2111 eyes with uveal melanomas, secondary IOP elevation was present in 55 (3%). Secondary IOP elevation was present in 7% of eyes with iris melanoma, 17% with ciliary body melanoma, and 2% with choroidal melanoma. The most common mechanism of elevated IOP was tumor invasion of the angle in the case of iris melanomas, pigment dispersion and tumor invasion of the angle in the case of ciliary body melanomas, and iris neovascularization in the case of choroidal melanomas. Of the 256 eyes with uveal metastases, secondary IOP elevation was found in 12 eyes (5%). Secondary IOP elevation was present in 64% of eyes with iris metastases, 67% with ciliary body metastases, and 1% with choroidal metastases. The most common mechanism of elevated IOP was tumor invasion of the angle in the case of iris and ciliary body metastases, and angle closure in the case of choroidal metastases. There were 303 eyes with retinoblastoma, 17% of which had elevated IOP which was secondary to iris neovascularization in 70% of cases and to an angle closure without neovascularization in 27%. Several other intraocular tumors including lymphoma, leukemia, medulloepithelioma, melanocytoma, and adenoma of the iris pigment epithelium were occasionally associated with secondary elevated IOP.
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PMID:Prevalence and mechanisms of secondary intraocular pressure elevation in eyes with intraocular tumors. 365 52

The molecular basis for parathyroid carcinoma remains undetermined. Parathyroid carcinoma potentially remains curable by early en bloc resection. This requires a reliable diagnostic tool as histological features alone are insufficient to distinguish parathyroid carcinoma from its benign counterpart, parathyroid adenoma. A variety of human cancers arise from the inactivation of the retinoblastoma (RB) gene, a tumour-suppressor gene on chromosome 13q14. We investigated the role of this gene in parathyroid growths by using a mouse monoclonal antibody to detect RB gene expression immunohistochemically. Two of the three parathyroid carcinomas in this study showed evidence of RB gene inactivation compared with one of 11 benign parathyroid entities. Three normal parathyroid glands stained showed strong evidence of RB gene expression in all three glands. The relationship between RB gene inactivation and parathyroid malignancy, however, was not statistically significant.
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PMID:Inactivation of retinoblastoma gene in malignant parathyroid growths: a candidate genetic trigger? 748 9

Over seven years (1983-1989), 30 orbital lesions were subjected to fine needle aspiration (FNA). The age of the patients ranged from 1.5 to 65 years. The male:female ratio was 16:14. The presenting features were proptosis (15 cases), swelling of eyelids (6), swelling of medial or lateral canthus (6), swelling of infraorbital margin (2) and recurrent orbital mass in a surgically treated case of retinoblastoma (1). FNA was performed on intraocular sites in 2 cases, orbital cavity in 11 and adnexal swellings in 17. The cytodiagnoses were various inflammatory lesions (5 cases), benign cystic lesions (4), meibomian gland carcinoma (3), retinoblastoma (3), meningioma (2) and pleomorphic adenoma (2). Basal cell carcinoma, mucoepidermoid carcinoma, undifferentiated carcinoma, optic nerve glioma, acute myeloid leukemia, leiomyosarcoma and neurofibroma accounted for 1 case each. In 4 cases the cytologic specimens were inadequate.
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PMID:Orbital lesions. Diagnosis by fine needle aspiration cytology. 814 5

Ca2+ and Ca(2+)-binding proteins are involved in running the cell cycle. Ca2+ spikes and signals from integrin-activated focal adhesion complexes and Ca2+ receptors on the cell surface along with cyclic AMP begin the cycle of cyclin-dependent protein kinases (PKs). These transiently expressed PKs stimulate the coordinate expression of DNA-replicating enzymes, activate replication enzymes, inactivate replication suppressors (e.g., retinoblastoma susceptibility protein), activate the replicator complexes at the end of the G1 build-up, and when replication is complete they and a Ca2+ spike trigger mitotic prophase. Another Ca2+ surge at the end of metaphase triggers the destruction of the prophase-stimulating PKs and starts anaphase. Ca2+ finally stimulates cytoplasmic division (cytokinesis). However, Ca2+ does more than this in epithelial cells, such as those lining the colon, and skin keratinocytes. These cells also need Ca2+, integrin signals, and only a small amount (e.g., 0.05-0.1 mM) of external Ca2+ to start DNA replication. Signals from their surface Ca2+ receptors trigger a combination of differentiation and apoptosis ("diffpoptosis") when external Ca2+ concentration reaches their setpoints. The skin's steep, upwardly directed, Ca2+ gradient has a low concentration in the basal layer to allow stem and precursor keratinocytes to proliferate, and higher concentrations in the suprabasal layers to trigger the differentiation-apoptosis ("diffpoptosis") mechanism that converts granular cells into protective, hard-shelled, dead corneocytes. A similar Ca2+ gradient may exist in the colon crypt allowing the stem cell and its amplifying transit or precursor offspring to cycle in the lower parts of the crypt, while stopping proliferation and stimulating terminal differentiation in the upper crypt and flat mucosa. Raising the amount of Ca2+ in fecal water above a critical level reduces proliferation and thus colorectal carcinogenesis in normal rats and some high-risk humans. But during carcinogenesis the Ca2+ sensors malfunction or their signals become ineffective: high Ca2+ does not stop, and may even stimulate, the proliferation of initiated mutants. Therefore, Ca2+ may either not affect, or even promote, the growth of epithelial cells in carcinogen-initiated rat colon and human adenoma patients. Clearly, a much greater understanding of how Ca2+ controls the proliferation and differentiation of epithelial cells and why initiated cells lose their responsiveness to Ca2+ are needed to assess the drawbacks and advantages of using Ca2+ as a chemopreventor.
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PMID:Calcium-cell cycle regulator, differentiator, killer, chemopreventor, and maybe, tumor promoter. 853 13


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